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Mechanism of anti-β-adrenoceptor antibody mediated myocardial damage in dilated cardiomyopathy

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Summary

Antibodies against β1-adrenoceptor can be detected in serum of patients with dilated cardiomyopathy (DCM), which have β-agonist-like activity, and induce a positive chronotropic effect on cardiac myocytes by its persistence at full strength. Effects of the antibodies against β-adrenoceptor from sera of patients with DCM on myocardial cytotoxicity and cytoplasmic free Ca2+-concentration ([Ca2+]i) were observed in the cultured single layer SD rat ventricular cells by using the cytotoxicity assay and fluorescent Ca2+- indicator fura-2/AM. The positive sera of the anti-β-adrenoceptor antibodies from patients with DCM markedly enhanced myocardial [Ca2+]i. Betaloc, a βi-receptor blocker, might inhibit the increase of the antibody-mediated myocardial [Ca2+]i, and the sera from healthy donors had no effect on myocardial [Ca2+]i. Our results suggest that the anti-β-adrenoceptor antibody might increase myocardial [Ca2+]i and result in myocardial damage. The antibodies might activate receptor-gating [Ca2+]-channel, thereby causing myocardial [Ca2+]i rise and calcium overload. Early use of betaloc is recommended in the treatment of dilated cardiomyopathy.

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This project was supported by the National Natural Science Fundation of China (No. 39370317).

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Yuhua, L., Longxian, C., Yuanshu, T. et al. Mechanism of anti-β-adrenoceptor antibody mediated myocardial damage in dilated cardiomyopathy. Current Medical Science 17, 5–8 (1997). https://doi.org/10.1007/BF02887992

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